Huntington's Cure? - Mitochondria & Mind - Targeting Tau - Magnetic Bees

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Jul 18, 2026, 6:24:41 AM (5 days ago) Jul 18

https://www.sciencenews.org/article/genes-huntingtons-therapy-expansion

Genes offer new clues to stopping Huntington’s disease in its tracks

By Elie Dolgin

Jeff Carroll was in his mid-twenties, fresh out of the U.S. Army, when a genetic test confirmed his worst fear: He was going to develop Huntington’s disease.

He had watched his mother’s illness for years; the tremors first, small enough to explain away, then the involuntary movements that looked almost like dancing. The test revealed that the same mutation that caused her disease lived in him: a stretch of three DNA letters in a gene called HTT, repeated over and over again dozens of times.

Carroll himself was not sick yet. He would not get sick for many years. But the countdown had begun. In fact, it had likely been running all his life, deep inside vulnerable neurons in his brain. There, the mutant HTT gene was slowly growing longer, its internal repeats piling up toward a threshold that, once crossed, would tip the cell into disarray.

The first outward signs of Huntington’s often begin with mood changes and subtle cognitive effects. The hallmark jerky movements come later. Eventually, and relentlessly, patients lose the ability to speak, swallow or move. Most people die within a decade or two of symptom onset.

Huntington’s disease is rare, affecting roughly 1 in 20,000 people worldwide. Yet because each child of an affected parent has a 50 percent chance of inheriting the mutation, the disease can haunt families for generations. It had already claimed Carroll’s grandmother and would take his mother at age 54. Without a therapy capable of altering its course, Carroll — along with three of his five siblings who also inherited the mutation — seemed fated to follow his ancestors into an early grave.

Carroll decided the only rational response was to become one of the scientists seeking ways to beat the disease. He was midway through his undergraduate studies when he learned, in 2003, that he carried the mutation. He pressed on, earning a Ph.D. and completing postdoctoral training before establishing his own research group devoted to understanding and slowing the disease stalking him from within.

https://www.theguardian.com/science/2026/jul/16/neural-bypass-brain-implant-paralysed-man-feed-himself-drink-from-cup

Brain implant helps paralysed man to feed himself and drink from cup

Ian Sample Science editor

A man who was paralysed from the chest down in a swimming accident six years ago has been able to feed himself and drink from a cup thanks to a brain implant that bypasses his spinal cord injury.

Keith Thomas of Massapequa, New York, could not lift his arms off his wheelchair when he agreed to trial the technology in 2021, but after surgery to implant electrodes in his brain and many months of training, he was able to move the limbs again.

Researchers fitted Thomas with a brain-computer interface that not only helped him move his arms and hands, but also sent signals back to his brain to recreate the sensation of touch. He has since been able to feel his sister’s hand and the fur on his pet dog.

Remarkably, the technology appears to have partly rewired Thomas’s nervous system, helping to restore some hand functions and sensations that remain even when the system is switched off.

“For me this is an incredible moment,” said Prof Chad Bouton, whose team developed the technology at the Feinstein Institutes for Medical Research, the research arm of the New York healthcare provider Northwell Health.

“For years, we have been wanting to really tackle the restoration of movement and the sense of touch and bring those together and we’ve also wanted to create lasting effects,” Bouton added. “I think we’re going to continue to see progress and I think it’ll be applicable to the millions of folks around the world who really need this technology.”

Thomas was 42 when he broke his neck diving into a swimming pool in July 2020. He blacked out and regained consciousness to see a helicopter on the front lawn. He was immediately taken to hospital. “The next day I couldn’t even move,” he said.

The following October, he joined a three-year clinical trial of what the researchers called a “double neural bypass”. It uses electrodes implanted into Thomas’s brain to detect when he wants to move his arms. The signals are then routed to his arms and hands to move them.

https://www.quantamagazine.org/martin-picards-mitochondrial-theory-of-mind-20260717/

Martin Picard’s Mitochondrial Theory of Mind

By Rachel Nuwer

It was 9 a.m. on a Thursday, and Martin Picard was watching his blood flow from an IV in his arm through a hole in the wall. He was sitting on a twin bed in a claustrophobic chamber less than a shoulder’s width from a stainless steel sink and porcelain toilet. Every hour over 24 hours, including while he slept, a nurse channeled blood from his arm to a research team next door; at each time point, if he was awake, he also provided a saliva sample and filled out a survey about his mood.

The room looked like a cell, or perhaps a very cramped hotel room, but in fact it was a metabolic research chamber, one of only 50 of its kind in the world. Its conspicuously small size prevented Picard from burning extra energy beyond the bare minimum needed to keep him alive. Napping during the day was prohibited, as was eating anything but the strictly scheduled meals tailored to his caloric needs. Bedtime was at 11 p.m. sharp. Before lights-out, Picard put on a device to monitor his vitals and brain activity while he slept.

Though there wasn’t much to do — mostly he sat in bed reading or working on his laptop — excitement was the primary emotion Picard felt that day in July 2021. That’s because he was the first volunteer in an experiment run by the Mitochondrial Psychobiology Lab (opens a new tab), which he directs at Columbia University Irving Medical Center in New York. By studying how much energy is required to sustain baseline existence, his lab aims to explore what he considers an overlooked factor in health and disease, from the level of molecules all the way up to the mind: mitochondria.

Most middle school students learn that mitochondria are the powerhouses of the cell. These organelles make adenosine triphosphate (ATP), the energy currency of life, through a cascade of chemical reactions that breaks down glucose and fat from food. But mitochondria are much more than energy factories. Studies over the past decade have shown that they process all sorts of molecules, including neurotransmitters, hormones, and metabolites, which means they directly impact what we experience as mood, stress, sexual arousal, and the need to sleep. This makes them “the consilience point for many known processes demonstrated to underlie consciousness,” Picard said.

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https://www.science.org/content/article/alzheimer-s-trial-results-lend-momentum-strategies-targeting-tau

Alzheimer’s trial results lend momentum to strategies targeting tau

By Jennie Erin Smith

Alzheimer’s disease has long been seen as a tale of two proteins: beta amyloid, which forms sticky plaques in the brain, and tau, which in its diseased state creates tangles inside neurons. Antibodies that clear beta amyloid have been approved to treat Alzheimer’s, but it was tau that made headlines this week, as researchers presented key new details about a drug that reduced production of the protein and slowed cognitive decline in a recent clinical trial.

At the Alzheimer’s Association International Conference, neurologist Catherine Mummery of University College London presented results from a phase 2 trial testing diranersen, a drug developed by Biogen to lower the body’s production of tau, in more than 400 patients with early-stage Alzheimer’s. On the study’s main measure of cognition, participants getting diranersen saw as much as a 26% slowing of decline—about on par with the effect seen in earlier trials of approved antiamyloid drugs. (Biogen had announced in May the drug slowed cognitive decline but did not say by how much.)

Although the presentation sparked enthusiasm from Alzheimer’s researchers, it also drew attention to puzzling aspects of the trial results. A potentially worrisome side effect emerged at high doses, and contrary to expectations, patients taking the lowest of three possible doses saw the greatest benefit. For these reasons, the findings represent “a double, not a home run,” says neurologist Adam Boxer of the University of California San Francisco, who this month launched a clinical trials platform to try different antitau therapies in Alzheimer’s.

Diranersen belongs to a class of drugs known as antisense oligonucleotides, strands of RNA that dampen activity of specific genes. It interrupts production of tau by binding to the messenger RNA that encodes instructions for producing the protein, and must be injected directly into the cerebrospinal fluid to reach the brain. After 18 months, participants in all three dose groups had between one-third and one-half as much tau in their cerebrospinal fluid as when they started the trial, whereas levels increased slightly among people receiving placebo. Imaging done on a subgroup of participants showed the drug also reduced tau tangles in the brain.

https://theconversation.com/bees-of-many-species-contain-tiny-magnetic-particles-suggesting-they-may-have-an-innate-magnetic-compass-for-navigation-282229

Bees of many species contain tiny magnetic particles – suggesting they may have an

Laura Russo

A surprisingly large number and diversity of bee species – 74 out of 96 tested – have magnetic properties, according to research my colleagues and I recently published in the journal Science Advances.

Some animals are able to use iron-based magnetic compounds such as magnetite to detect and navigate via the Earth’s magnetic field – a sense called magnetoreception. We considered magnetism in the insects we tested to be a proxy for which species might be magnetoreceptive.

For decades, biologists have known that social, cavity-nesting honeybees exhibit magnetoreception. Most researchers assumed that this internal compass was tied to living in a colony; honeybees communicate the location of floral resources to other colony members through a dance that indicates direction relative to the position of the Sun and the geomagnetic field.

Our study had two goals: to compare magnetism between bee species that live in groups versus on their own, and to track down the evolutionary origin of magnetoreception in bees.

To test magnetic responses, we collected bee specimens from across the bee family Apidae, which includes social species such as honeybees along with solitary species such as chimney bees. We ground dried dead bees into a powder, then measured how magnetic this powder was in a magnetometer.

To our surprise, we found that the magnetic response was strong in both bees that live in groups and those that live alone. This result forced us to reject our initial hypothesis that magnetism was necessary only for social bee species.
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© 2010–2026, The Conversation US, Inc.

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https://www.thetransmitter.org/sleep/making-waves-sleep-like-brain-activity-in-awake-mice-lowers-sleep-need-boosts-memory/

Making waves: Sleep-like brain activity in awake mice lowers sleep need, boosts memory

By Alissa de Chassey

A hallmark of deep sleep—slow-wave brain activity that arises when cortical neurons cycle on and off synchronously between 0.5 and 4 Hertz—may drive some of sleep’s restorative functions, according to a new study published last month in Nature Neuroscience.

“We provided direct evidence that these on and off patterns are what really matter,” says study investigator Chiara Cirelli, professor of psychiatry at the University of Wisconsin School of Medicine.

As slow waves travel across the cortex during deep sleep, the excitatory synaptic strength that accrued during waking hours gradually returns to a baseline, a process that helps to consolidate memories, according to the synaptic homeostasis hypothesis of sleep that Cirelli and her husband, neuroscientist Giulio Tononi, proposed more than two decades ago. Computational models and studies of anesthetized animals support the idea, but the field has lacked evidence from non-anesthetized animals.

“Anesthesia and sleep may share some features, but definitely overall they are not the same thing,” Cirelli says.

She and her colleagues used optogenetics to induce sleep-like on/off firing patterns in select regions of the cortex in awake mice. “The idea was to induce these patterns in awake mice, and see whether this is enough to get sleep benefits,” Cirelli says.

As expected, the animals showed a decreased need for sleep; reduced neuronal synchrony and synaptic strength during sleep; and improved memory consolidation afterward.